Impaired ammonia metabolism in severe hepatic disease

CLINICA

BRIEF

CHIMICA

181

ACTA

NOTES

Impaired ammonia

metabolism

in severe hepatic disease

In severe hepatic insufficiency the metabolic efficiency of the liver cells is more or less impaired. In particular, ammonia detoxication through ureogenesis seems to be one of the processes most affected. In fact, when the liver damage reaches a certain degree, the rate of ammonia production, mainly through oxidative deamination of amino acids, esceeds the conversion of ammonia into urea1-4. The present communication refers to some results obtained in following blood ammonia level in normal and in cirrhotic patients after intravenous glycine administration (Fig. I). The results reported in Table I show that in patients with non-hepatic diseases blood ammonia level is not modified by glycine administration. On the contrary in all hepatic patients (6 with alcoholic cirrhosis, r with post-hepatic cirrhosis, and r with metastatic cancer of the liver) blood ammonia increases significantly above the initial values 15 min after glycine administration and the increased level lasts in some subjects for more than I hour. It has to be emphasised that the “basal” level of ammonia in hepatic patients is constantly higher than in normal subjects. These results clearly show that the inability to convert ammonia into urea at

i

182

a rate comparable metabolic

alteration

with that of its formation in human

\\:e wis1~ to tliank Chemistry (I’niversity

l;iasclli,

from amino acids represents

a constant

disease.

Prof. Km-is Siliprandi,

arid l’rof. Ernico of Padova)

hepatic

Director

for the help gixm.

Director

of tire Institute

of the Institute

of LZiological

of l\lcdicxl I’atldog!